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      Serum IL-33 as a biomarker in different diseases: useful parameter or much need for clarification?

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          ABSTRACT

          Interleukin-33 (IL-33), a member of the IL-1 family, is critically involved in the modulation of the activity of a diverse range of immunocompetent cells. Essential roles have been implicated in cardioprotection, in both innate and adaptive immune responses in mucosal organs, and in the maintenance of adipose tissue cells. Over the past 10 years, several studies evaluated the usability of IL-33 as a biomarker in diseases of inflammatory and noninflammatory origin. Our group is currently evaluating the predictive role of serum IL-33 in acute kidney injury (AKI). The aim of the article is to discuss selected studies on IL-33 in different diseases and its potential role as a biomarker molecule.

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          Interleukin-33 (IL-33): A nuclear cytokine from the IL-1 family.

          Jean-Philippe Girard, Corinne Cayrol (2018)
          Interleukin-33 (IL-33) is a tissue-derived nuclear cytokine from the IL-1 family abundantly expressed in endothelial cells, epithelial cells and fibroblast-like cells, both during homeostasis and inflammation. It functions as an alarm signal (alarmin) released upon cell injury or tissue damage to alert immune cells expressing the ST2 receptor (IL-1RL1). The major targets of IL-33 in vivo are tissue-resident immune cells such as mast cells, group 2 innate lymphoid cells (ILC2s) and regulatory T cells (Tregs). Other cellular targets include T helper 2 (Th2) cells, eosinophils, basophils, dendritic cells, Th1 cells, CD8+T cells, NK cells, iNKT cells, B cells, neutrophils and macrophages. IL-33 is thus emerging as a crucial immune modulator with pleiotropic activities in type-2, type-1 and regulatory immune responses, and important roles in allergic, fibrotic, infectious, and chronic inflammatory diseases. The critical function of IL-33/ST2 signaling in allergic inflammation is illustrated by the fact that IL33 and IL1RL1 are among the most highly replicated susceptibility loci for asthma. In this review, we highlight 15 years of discoveries on IL-33 protein, including its molecular characteristics, nuclear localization, bioactive forms, cellular sources, mechanisms of release and regulation by proteases. Importantly, we emphasize data that have been validated using IL-33-deficient cells.
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            Biomarkers in acute kidney injury - pathophysiological basis and clinical performance.

            EV. Schrezenmeier, J Barasch, K Budde … (2017)
            Various biomarkers of acute kidney injury (AKI) have been discovered and characterized in the recent past. These molecules can be detected in urine or blood and signify structural damage to the kidney. Clinically, they are proposed as adjunct diagnostics to serum creatinine and urinary output to improve the early detection, differential diagnosis and prognostic assessment of AKI. The most obvious requirements for a biomarker include its reflection of the underlying pathophysiology of the disease. Hence, a biomarker of AKI should derive from the injured kidney and reflect a molecular process intimately connected with tissue injury. Here, we provide an overview of the basic pathophysiology, the cellular sources and the clinical performance of the most important currently proposed biomarkers of AKI: neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), liver-type fatty acid-binding protein (L-FABP), interleukin-18 (IL-18), insulin-like growth factor-binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinase 2 (TIMP-2) and calprotectin (S100A8/9). We also acknowledge each biomarker's advantages and disadvantages as well as important knowledge gaps and perspectives for future studies.
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              Structural Basis of IL-1 Family Cytokine Signaling

              James Fields, Sebastian Günther, Eric J Sundberg (2019)
              Interleukin-1 (IL-1) family cytokines are key signaling molecules in both the innate and adaptive immune systems, mediating inflammation in response to a wide range of stimuli. The basic mechanism of signal initiation is a stepwise process in which an agonist cytokine binds its cognate receptor. Together, this cytokine-receptor complex recruits an often-common secondary receptor. Intracellularly, the Toll/IL-1 Receptor (TIR) domains of the two receptors are brought into close proximity, initiating an NF-κB signal transduction cascade. Due to the potent inflammatory response invoked by IL-1 family cytokines, several physiological mechanisms exist to inhibit IL-1 family signaling, including antagonist cytokines and decoy receptors. The numerous cytokines and receptors in the IL-1 superfamily are further classified into four subfamilies, dependent on their distinct cognate receptors—the IL-1, IL-33, and IL-36 subfamilies share IL-1RAcP as their secondary receptor, while IL-18 subfamily utilizes a distinct secondary receptor. Here, we describe how structural biology has informed our understanding of IL-1 family cytokine signaling, with a particular focus on molecular mechanisms of signaling complex formation and antagonism at the atomic level, as well as how these findings have advanced therapeutics to treat some chronic inflammatory diseases that are the result of dysregulated IL-1 signaling.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Circ Biomark
                Journal ID (iso-abbrev): J Circ Biomark
                Journal ID (publisher-id): JCB
                Title: Journal of Circulating Biomarkers
                Publisher: AboutScience
                ISSN (Electronic): 1849-4544
                Publication date (Electronic): 30 November 2021
                Publication date Collection: Jan-Dec 2021
                Volume: 10 ,2021
                Pages: 20-25
                Affiliations
                [1 ] Department of Medicine 1, University Hospital Brandenburg, Medical School (MHB) Theodor Fontane, Brandenburg - Germany
                [2 ] Institute of Biochemistry, Brandenburg Medical School (MHB) Theodor Fontane, Brandenburg - Germany
                Author notes
                Corresponding author: Zentrum Innere Medizin 1 Universitätsklinikum Brandenburg Medizinische Hochschule Brandenburg Hochstraße 29 14770 Brandenburg - Germany daniel.patschan@mhb-fontane.de
                Article
                DOI: 10.33393/jcb.2021.2327
                PMC ID: 8634375
                PubMed ID: 34858526
                SO-VID: 4051288d-cf2b-4ff1-8864-b7473f046b42
                Copyright © Copyright © 2021, The Authors
                License:

                Journal of Circulating Biomarkers - ISSN 1849-4544 - www.aboutscience.eu/jcb

                © 2021 The Authors. This article is published by AboutScience and licensed under Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Commercial use is not permitted and is subject to Publisher’s permissions. Full information is available at www.aboutscience.eu

                History
                Date received : 3 August 2021
                Date accepted : 10 November 2021
                Categories
                Subject: Review

                Keywords: biomarker,il-33,inflammatory diseases,noninflammatory diseases
                Data availability:
                Keywords: biomarker, il-33, inflammatory diseases, noninflammatory diseases

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